Krüppel-like factor 9 inhibits glioma cell proliferation and tumorigenicity via downregulation of miR-21
Autor: | Xiao-dan Jiang, Xinlin Sun, Shuyun Huang, Ying-qian Cai, Zhen-jun Zhou, Chanjuan Wang, Jianwen Li, Yongjun Yi, Min-jie Luo, Yiquan Ke |
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Rok vydání: | 2015 |
Předmět: |
Cancer Research
Cell cycle checkpoint Blotting Western Kruppel-Like Transcription Factors Apoptosis Biology Real-Time Polymerase Chain Reaction medicine.disease_cause Immunoenzyme Techniques Mice Glioma microRNA Cell Adhesion Tumor Cells Cultured medicine Animals Humans RNA Messenger Promoter Regions Genetic Transcription factor Cell Proliferation Regulation of gene expression Mice Inbred BALB C Reverse Transcriptase Polymerase Chain Reaction Cell growth Flow Cytometry medicine.disease Xenograft Model Antitumor Assays Molecular biology Gene Expression Regulation Neoplastic MicroRNAs KLF9 Cell Transformation Neoplastic Oncology Astrocytes Cancer research Carcinogenesis |
Zdroj: | Cancer Letters. 356:547-555 |
ISSN: | 0304-3835 |
Popis: | Krüppel-like factors (KLFs) are zinc finger-containing transcription factors that play key roles in the regulation of differentiation and development as well as biological processes central to the development of malignancies. Increasing evidence indicates that Krüppel-like factor 9 (KLF9) plays a critical role in regulating tumorigenesis. However, the biological role and molecular mechanism of KLF9 in glioma progression remain unclear. Herein, we found that KLF9 expression was strongly reduced in gliomas. Reduced KLF9 expression promoted glioma cell proliferation. Importantly, re-constitution of KLF9 expression inhibited glioma cell proliferation and tumor growth in vivo. Furthermore, we determined that KLF9 interacted with the miR-21 promoter, leading to suppression of miR-21 expression and cell cycle arrest. Taken together, our findings indicate a novel mechanism for KLF function in tumorigenesis and may also suggest new targets for clinical intervention in human cancer. |
Databáze: | OpenAIRE |
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